Peptidomic analysis on synovial tissue reveals galectin-1 derived peptide as a potential bioactive molecule against rheumatoid arthritis

• Published in: Cytokine (Philadelphia, Pa.) Vol. 131; p. 155020
• Main Authors: Hu, Junzheng, Lu, Jun, Zhang, Xiao, Wang, Chen, Ren, Ke, Chang, Qing, Ji, Mingliang, Pan, Wei, Ma, BinBin, Fan, Weimin
• Format: Journal Article
• Language: English
• Published: England Elsevier Ltd 01-07-2020
• Subjects: Bioactive peptide; Inflammatory; LC-MS/MS; MH7A; Peptidomics; Synovial fibroblast; TNF-α; CC; PBS; MH7A; CPP; Bioactive peptide; GO; PPI; Peptidomics; IL-1β; TNF; IL-6; BP; RA; LC-MS/MS; Synovial fibroblast; RASFs; TNF-α; UPP; MMP-1; Inflammatory; KEGG; TGF-β; G1dps; G1dp3
• ISSN: 1043-4666; 1096-0023
• DOI: 10.1016/j.cyto.2020.155020

•We aimed to reveal pathogenesis of RA in peptidomic perspective.•Bioinformatics analyses disclosed the roles of differentially peptides in RA.•A galectin-1 derived peptide inhibited abnormal proliferation of synovial cells.
Rheumatoid arthritis (RA) is an autoimmune disease that leads to small joints irreversible destruction. Despite intense efforts, the pathophysiology of RA currently remains unclear. We aimed to gain insight into the pathophysiology process in peptidomic perspective and to identify bioactive peptides for RA treatment.
The endogenous peptides in synovial tissue between control and rheumatoid arthritis group were identified by liquid chromatography-mass spectrometry (LC-MS/MS). Since the biological function of peptides were always associated with precursor proteins, the potential function of the differentially peptides were predicted by GO and pathway analysis of their precursors. Besides, peptides located in the domains of their precursors were identified. Finally, we determined the impact of galectin-1 derived peptide by administration on the damage to MH7A cells caused by TNF-α.
Totally, 141 down-regulated peptides and 10 up-regulated peptides were identified (Fold change > 1.5 and P < 0.05). It indicated that these differentially peptides were tightly involved in the pathophysiology process of RA preliminarily. Finally, we identified a peptide derived from the domain of galectin-1 could inhibit the abnormal proliferation induced by TNF-α and promoted apoptosis of MH7A.
In summary, our study provided a better understanding of endogenous peptides in RA. We found a peptide that might be used in anti-RA treatment.